We intend to determine what chemical mediators are released, and in what sequence during different types of ocular inflammation produced by nitrogen mustard, formaldehyde, paracentesis and types I, II, III and IV immunogenic reactions. We will measure the release of prostaglandins, histamine and kinins. We will also investigate the interactions of prostaglandins with these other mediators of inflammation both in intraocular (uveitis) and extraocular (conjunctivitis) inflammation. We are particularly interested in the mediator of the atropine-resistant meiosis produced by trauma in the rabbit eye. We will determine the ocular effects of prostaglandin intermediates (such as the endoperoxides), PG analogues (such as 16, 16 dimethyl PGE2) and PG metabolites (such as 15-keto PGE2). Finally, we will investigate the relationship between steroidal anti-inflammatory agents and the PG-generating systems of ocular tissues. These studies will enable us to better evaluate the role of PGs in ocular disease, particularly ocular inflammation. A rational approach to the therapeutic control of ocular inflammation requires a clear understanding of the processes involved so that the best anti-inflammatory agent (or combination of agents) may be selected for use.